scholarly journals Unhealthy Lifestyle, Genetics and Risk of Cardiovascular Disease and Mortality in 76,958 Individuals from the UK Biobank Cohort Study

Nutrients ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 4283
Author(s):  
Katherine M. Livingstone ◽  
Gavin Abbott ◽  
Joey Ward ◽  
Steven J. Bowe

To examine associations of unhealthy lifestyle and genetics with risk of all-cause mortality, cardiovascular disease (CVD) mortality, myocardial infarction (MI) and stroke. We used data on 76,958 adults from the UK Biobank prospective cohort study. Favourable lifestyle included no overweight/obesity, not smoking, physical activity, not sedentary, healthy diet and adequate sleep. A Polygenic Risk Score (PRS) was derived using 300 CVD-related single nucleotide polymorphisms. Cox proportional hazard ratios (HR) were used to model effects of lifestyle and PRS on risk of CVD and all-cause mortality, stroke and MI. New CVD (n = 364) and all-cause (n = 2408) deaths, and stroke (n = 748) and MI (n = 1140) events were observed during a 7.8 year mean follow-up. An unfavourable lifestyle (0–1 healthy behaviours) was associated with higher risk of all-cause mortality (HR: 2.06; 95% CI: 1.73, 2.45), CVD mortality (HR: 2.48; 95% CI: 1.64, 3.76), MI (HR: 2.12; 95% CI: 1.65, 2.72) and stroke (HR:1.74; 95% CI: 1.25, 2.43) compared to a favourable lifestyle (≥4 healthy behaviours). PRS was associated with MI (HR: 1.35; 95% CI: 1.27, 1.43). There was evidence of a lifestyle-genetics interaction for stroke (p = 0.017). Unfavourable lifestyle behaviours predicted higher risk of all-cause mortality, CVD mortality, MI and stroke, independent of genetic risk.

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
D Radenkovic ◽  
S.C Chawla ◽  
G Botta ◽  
A Boli ◽  
M.B Banach ◽  
...  

Abstract   The two leading causes of mortality worldwide are cardiovascular disease (CVD) and cancer. The annual total cost of CVD and cancer is an estimated $844.4 billion in the US and is projected to double by 2030. Thus, there has been an increased shift to preventive medicine to improve health outcomes and development of risk scores, which allow early identification of individuals at risk to target personalised interventions and prevent disease. Our aim was to define a Risk Score R(x) which, given the baseline characteristics of a given individual, outputs the relative risk for composite CVD, cancer incidence and all-cause mortality. A non-linear model was used to calculate risk scores based on the participants of the UK Biobank (= 502548). The model used parameters including patient characteristics (age, sex, ethnicity), baseline conditions, lifestyle factors of diet and physical activity, blood pressure, metabolic markers and advanced lipid variables, including ApoA and ApoB and lipoprotein(a), as input. The risk score was defined by normalising the risk function by a fixed value, the average risk of the training set. To fit the non-linear model >400,000 participants were used as training set and >45,000 participants were used as test set for validation. The exponent of risk function was represented as a multilayer neural network. This allowed capturing interdependent behaviour of covariates, training a single model for all outcomes, and preserving heterogeneity of the groups, which is in contrast to CoxPH models which are traditionally used in risk scores and require homogeneous groups. The model was trained over 60 epochs and predictive performance was determined by the C-index with standard errors and confidence intervals estimated with bootstrap sampling. By inputing the variables described, one can obtain personalised hazard ratios for 3 major outcomes of CVD, cancer and all-cause mortality. Therefore, an individual with a risk Score of e.g. 1.5, at any time he/she has 50% more chances than average of experiencing the corresponding event. The proposed model showed the following discrimination, for risk of CVD (C-index = 0.8006), cancer incidence (C-index = 0.6907), and all-cause mortality (C-index = 0.7770) on the validation set. The CVD model is particularly strong (C-index >0.8) and is an improvement on a previous CVD risk prediction model also based on classical risk factors with total cholesterol and HDL-c on the UK Biobank data (C-index = 0.7444) published last year (Welsh et al. 2019). Unlike classically-used CoxPH models, our model considers correlation of variables as shown by the table of the values of correlation in Figure 1. This is an accurate model that is based on the most comprehensive set of patient characteristics and biomarkers, allowing clinicians to identify multiple targets for improvement and practice active preventive cardiology in the era of precision medicine. Figure 1. Correlation of variables in the R(x) Funding Acknowledgement Type of funding source: None


BMJ ◽  
2020 ◽  
pp. m456 ◽  
Author(s):  
Zhi-Hao Li ◽  
Wen-Fang Zhong ◽  
Simin Liu ◽  
Virginia Byers Kraus ◽  
Yu-Jie Zhang ◽  
...  

Abstract Objectives To evaluate the associations of habitual fish oil supplementation with cardiovascular disease (CVD) and mortality in a large prospective cohort. Design Population based, prospective cohort study. Setting UK Biobank. Participants A total of 427 678 men and women aged between 40 and 69 who had no CVD or cancer at baseline were enrolled between 2006 and 2010 and followed up to the end of 2018. Main exposure All participants answered questions on the habitual use of supplements, including fish oil. Main outcome measures All cause mortality, CVD mortality, and CVD events. Results At baseline, 133 438 (31.2%) of the 427 678 participants reported habitual use of fish oil supplements. The multivariable adjusted hazard ratios for habitual users of fish oil versus non-users were 0.87 (95% confidence interval 0.83 to 0.90) for all cause mortality, 0.84 (0.78 to 0.91) for CVD mortality, and 0.93 (0.90 to 0.96) for incident CVD events. For CVD events, the association seemed to be stronger among those with prevalent hypertension (P for interaction=0.005). Conclusions Habitual use of fish oil seems to be associated with a lower risk of all cause and CVD mortality and to provide a marginal benefit against CVD events among the general population.


2022 ◽  
Vol 97 (1) ◽  
pp. 110-121
Author(s):  
Irene Rodríguez-Gómez ◽  
Stuart R. Gray ◽  
Frederick K. Ho ◽  
Fanny Petermann-Rocha ◽  
Paul Welsh ◽  
...  

BMJ Open ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. e045362
Author(s):  
Katherine M Livingstone ◽  
Gavin Abbott ◽  
Steven J Bowe ◽  
Joey Ward ◽  
Catherine Milte ◽  
...  

ObjectivesTo examine associations of three diet quality indices and a polygenic risk score with incidence of all-cause mortality, cardiovascular disease (CVD) mortality, myocardial infarction (MI) and stroke.DesignProspective cohort study.SettingUK Biobank, UK.Participants77 004 men and women (40–70 years) recruited between 2006 and 2010.Main outcome measuresA polygenic risk score was created from 300 single nucleotide polymorphisms associated with CVD. Cox proportional HRs were used to estimate independent effects of diet quality and genetic risk on all-cause mortality, CVD mortality, MI and stroke risk. Dietary intake (Oxford WebQ) was used to calculate Recommended Food Score (RFS), Healthy Diet Indicator (HDI) and Mediterranean Diet Score (MDS).ResultsNew all-cause (n=2409) and CVD (n=364) deaths and MI (n=1141) and stroke (n=748) events were identified during mean follow-ups of 7.9 and 7.8 years, respectively. The adjusted HR associated with one-point higher RFS for all-cause mortality was 0.96 (95% CI: 0.94 to 0.98), CVD mortality was 0.94 (95% CI: 0.90 to 0.98), MI was 0.97 (95% CI: 0.95 to 1.00) and stroke was 0.94 (95% CI: 0.91 to 0.98). The adjusted HR for all-cause mortality associated with one-point higher HDI and MDS was 0.97 (95% CI: 0.93 to 0.99) and 0.95 (95% CI: 0.91 to 0.98), respectively. The adjusted HR associated with one-point higher MDS for stroke was 0.93 (95% CI: 0.87 to 1.00). There was little evidence of associations between HDI and risk of CVD mortality, MI or stroke. There was evidence of an interaction between diet quality and genetic risk score for MI.ConclusionHigher diet quality predicted lower risk of all-cause mortality, independent of genetic risk. Higher RFS was also associated with lower risk of CVD mortality and MI. These findings demonstrate the benefit of following a healthy diet, regardless of genetic risk.


2018 ◽  
Vol 120 (4) ◽  
pp. 464-471 ◽  
Author(s):  
Emiko Okada ◽  
Koshi Nakamura ◽  
Shigekazu Ukawa ◽  
Kenji Wakai ◽  
Chigusa Date ◽  
...  

AbstractFew studies have reported the association between the Japanese diet as food score and mortality. This study aimed to investigate adherence to the Japanese food score associated with all-cause, CVD and cancer mortality. A total of 58 767 (23 162 men and 34 232 women) Japanese participants aged 40–79 years, who enrolled in the Japan Collaborative Cohort Study between 1988 and 1990, were included. The Japanese food score was derived from the components of seven food groups (beans and bean products, fresh fishes, vegetables, Japanese pickles, fungi, seaweeds and fruits) based on the FFQ. The total score ranged from 0 to 7, and participants were divided into five categories based on scores (0–2, 3, 4, 5 and 6–7). Hazard ratios (HR) and 95 % CI for all-cause, CVD and cancer mortality based on sex were estimated using Cox proportional models. During the follow-up period until 2009, 11 692 participants with all-cause, 3408 with CVD and 4247 with cancer died. The multivariable HR in the 6–7 and 0–2 Japanese food score groups were 0·93 (95 % CI 0·86, 1·01) in men and 0·82 (95 % CI 0·75, 0·90) in women for all-cause mortality and 0·89 (95 % CI 0·76, 1·04) in men and 0·66 (95 % CI 0·56, 0·77) in women for CVD mortality. Our findings suggest that adherence to the Japanese food score consisting of food combinations characterised by a Japanese diet may help in preventing all-cause and CVD mortality, especially in women.


BMJ ◽  
2020 ◽  
pp. m34 ◽  
Author(s):  
Ryoko Katagiri ◽  
Norie Sawada ◽  
Atsushi Goto ◽  
Taiki Yamaji ◽  
Motoki Iwasaki ◽  
...  

Abstract Objective To investigate the association between several types of soy products and all cause and cause specific mortality. Design Population based cohort study. Setting Japan Public Health Centre-based Prospective Study, which includes 11 public health centre areas in Japan. Participants 92 915 participants (42 750 men and 50 165 women) aged 45 to 74 years. Exposures Intake of total soy products, fermented soy products (natto and miso), non-fermented soy products, and tofu from a five year survey questionnaire. Main outcome measures All cause and cause specific mortality (cancer, total cardiovascular disease, heart disease, cerebrovascular disease, respiratory disease, and injury) obtained from residential registries and death certificates. Results During 14.8 years of follow-up, 13 303 deaths were identified. In the multivariable adjusted models, intake of total soy products was not significantly associated with total mortality. Compared with the lowest fifth of total soy product intake, the hazard ratios in the highest fifth were 0.98 (95% confidence interval 0.91 to 1.06, P trend =0.43) in men and 0.98 (0.89 to 1.08, P trend =0.46) in women. Intake of fermented soy products was inversely associated with all cause mortality in both sexes (highest versus lowest fifth: 0.90 (0.83 to 0.97), P trend =0.05 in men, and 0.89 (0.80 to 0.98), P trend =0.01 in women). Natto showed significant and inverse associations with total cardiovascular disease related mortality in both sexes. Conclusions In this study a higher intake of fermented soy was associated with a lower risk of mortality. A significant association between intake of total soy products and all cause mortality was not, however, observed. The findings should be interpreted with caution because the significant association of fermented soy products might be attenuated by unadjusted residual confounding.


2021 ◽  
pp. 1-24
Author(s):  
Briar L McKenzie ◽  
Katie Harris ◽  
Sanne A E Peters ◽  
Jacqui Webster ◽  
Mark Woodward

Abstract This study aimed to investigate the association between individual, and combinations of, macronutrients with premature death, cardiovascular disease (CVD) and dementia. Sex differences were investigated. Data were utilised from a prospective cohort of 120,963 individuals (57% female) within the UK Biobank, who completed ≥two 24-hour diet recalls. The associations of macronutrients, as percentages of total energy intake, with outcomes were investigated. Combinations of macronutrients were defined using k-means cluster analysis, with clusters explored in association with outcomes. There was a higher risk of death with high carbohydrate intake (Hazard ratios (HRs), 95% confidence intervals (95% CI) upper v lowest third 1.13 (1.03, 1.23)), yet a lower risk with higher intakes of protein (upper v lowest third 0.82 (0.76, 0.89)). There was a lower risk of CVD with moderate intakes (middle v lowest third) of energy and protein (sub distribution HRs (SHR), 0.87 (0.79, 0.97) and (0.87 (0.79, 0.96)) respectively). There was a lower risk of dementia with moderate energy intake (SHR 0.71 (0.52, 0.96)). Sex differences were identified. The dietary cluster characterised by low carbohydrate, low fat and high protein was associated with a lower risk of death (HR 0.84 (0.76, 0.93)) compared to the reference cluster, and a lower risk of CVD for men (SHR 0.83 (0.71, 0.97)). Given that associations were evident, both as single macronutrients and for combinations with other macronutrients for death, and for CVD in men, we suggest that the biggest benefit from diet-related policy and interventions will be when combinations of macronutrients are targeted.


2021 ◽  
Vol 8 ◽  
Author(s):  
Jiang-lin Wang ◽  
Wen-jun Yin ◽  
Ling-yun Zhou ◽  
Ya-feng Wang ◽  
Xiao-cong Zuo

Objectives: To examine the effect of smoking status, smoking intensity, duration of smoking cessation and age of smoking initiation on the risk of all-cause and cause-specific mortality among cardiovascular disease (CVD) patients.Design: A population-based prospective cohort study.Setting: The National Health Interview Survey (NHIS) in the U.S. that were linked to the National Death Index (NDI).Participants: 66,190 CVD participants ≥ 18 years of age who were interviewed between 1997 and 2013 in the NHIS linked to the NDI through December 31, 2015.Outcome Measures: The primary outcome was all-cause mortality and the secondary outcome was cause-specific mortality including CVD mortality and cancer mortality.Results: During the mean follow-up of 8.1 years, we documented 22,518 deaths (including 6,473 CVD deaths and 4,050 cancer deaths). In the overall CVD population, former and current smokers had higher risk of all-cause (Former smokers: hazard ratios (HRs), 1.26; 95% confidence interval (CI), 1.21–1.31, P < 0.001; Current smokers: HRs, 1.96; 95%CI, 1.86–2.07, P < 0.001), CVD (Former smokers: HRs, 1.12; 95%CI, 1.05–1.21, P = 0.001; Current smokers: HRs, 1.80; 95%CI, 1.64–1.97, P < 0.001) and cancer mortality (Former smokers: HRs, 1.49; 95%CI, 1.35–1.64, P < 0.001; Current smokers: HRs, 2.78; 95%CI, 2.49–3.09, P < 0.001) than never smokers. Furthermore, similar results were observed when the study subjects were stratified according to the type of CVD. Among current smokers, the risk for cancer mortality increased as the daily number of cigarettes increased, regardless of the specific type of CVD. However, the association of the risk for all-cause and CVD mortality with smoking intensity did not present a dose-response relationship. In participants with angina pectoris or stroke, smoking intensity was inversely associated with deaths from CVD. In addition, the risk for all-cause, CVD and cancer mortality declined as years of smoking cessation increased. Finally, the relative risk of all-cause mortality was not significantly different in individuals with a younger age of smoking initiation.Conclusions: CVD patients who are smokers have an increased risk of all-cause, CVD and cancer mortality, and the risk decreases significantly after quitting smoking. These data further provide strong evidence that supports the recommendation to quit smoking for the prevention of premature deaths among individuals with CVD.


BMJ ◽  
2020 ◽  
pp. m131 ◽  
Author(s):  
G David Batty ◽  
Catharine R Gale ◽  
Mika Kivimäki ◽  
Ian J Deary ◽  
Steven Bell

AbstractObjectiveTo compare established associations between risk factors and mortality in UK Biobank, a study with an exceptionally low rate of response to its baseline survey, against those from representative studies that have conventional response rates.DesignProspective cohort study alongside individual participant meta-analysis of other cohort studies.SettingUnited Kingdom.ParticipantsAnalytical sample of 499 701 people (response rate 5.5%) in analyses in UK Biobank; pooled data from the Health Surveys for England (HSE) and the Scottish Health Surveys (SHS), including 18 studies and 89 895 people (mean response rate 68%). Both study populations were linked to the same nationwide mortality registries, and the baseline age range was aligned at 40-69 years.Main outcome measureDeath from cardiovascular disease, selected malignancies, and suicide. To quantify the difference between hazard ratios in the two studies, a ratio of the hazard ratios was used with HSE-SHS as the referent.ResultsRisk factor levels and mortality rates were typically more favourable in UK Biobank participants relative to the HSE-SHS consortium. For the associations between risk factors and mortality endpoints, however, close agreement was seen between studies. Based on 14 288 deaths during an average of 7.0 years of follow-up in UK Biobank and 7861 deaths over 10 years of mortality surveillance in HSE-SHS, for cardiovascular disease mortality, for instance, the age and sex adjusted hazard ratio for ever having smoked cigarettes (versus never) was 2.04 (95% confidence interval 1.87 to 2.24) in UK Biobank and 1.99 (1.78 to 2.23) in HSE-SHS, yielding a ratio of hazard ratios close to unity (1.02, 0.88 to 1.19). The overall pattern of agreement between studies was essentially unchanged when results were compared separately by sex and when baseline years and censoring dates were aligned.ConclusionDespite a very low response rate, risk factor associations in the UK Biobank seem to be generalisable.


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